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The adrenal cortex is organised into functionally distinct zones:
the outer glomerulosa produces aldosterone,
the fasciculata produces cortisol and the reticularis produces androgens;
catecholamines originate in the separate medulla.
Cortisol and androgens answer to ACTH,
whereas aldosterone answers to the renin-angiotensin system and to potassium.
Secondary adrenal insufficiency from pituitary failure spares aldosterone,
and hyperkalaemia with hyponatraemia points to destruction of the gland itself.
Cushing's syndrome is diagnosed in three steps: confirm excess, measure ACTH,
then localise.
Because cortisol is circadian, a random level proves nothing;
screening must bypass the rhythm.
An overnight 1 mg dexamethasone test should suppress morning cortisol below 50 nmol/L;
24-hour urinary free cortisol integrates the day,
and late-night salivary cortisol captures a lost nadir.
A suppressed ACTH indicates an adrenal source or exogenous steroid;
a normal or high ACTH indicates a pituitary adenoma or ectopic secretion,
classically small cell lung cancer.
High-dose dexamethasone suppresses pituitary tumours but not ectopic sources.
The cushingoid patient whose ACTH,
cortisol
and urinary cortisol are all low is taking a synthetic glucocorticoid that
the assay cannot see.
The adrenal cortex is organised into functionally distinct zones:
the outer glomerulosa produces aldosterone,
the fasciculata produces cortisol and the reticularis produces androgens;
catecholamines originate in the separate medulla.
Primary aldosteronism is the most common endocrine cause of secondary hypertension,
affecting at least 5 per cent of hypertensives.
Autonomous aldosterone acts on ENaC in collecting duct principal cells,
retaining sodium while potassium and hydrogen are lost.
Hypokalaemia, metabolic alkalosis and volume expansion follow,
and the expanded volume suppresses renin.
Aldosterone escape within one to two weeks prevents oedema,
yet hypertension and hypokalaemia persist.
Screening uses the aldosterone-to-renin ratio,
drawn in the morning after two hours upright, with potassium corrected first,
since hypokalaemia suppresses aldosterone.
Mineralocorticoid antagonists are withheld for four weeks and ACE inhibitors, angiotensin blockers,
dihydropyridines and beta-blockers for two, with verapamil,
hydralazine or an alpha-blocker as cover.
A saline infusion of 2 litres over four hours confirms the diagnosis
when aldosterone remains above 277 pmol/L.
Adrenal vein sampling then separates a unilateral adenoma, cured by laparoscopic adrenalectomy,
from bilateral hyperplasia, controlled by spironolactone; in renovascular disease, by contrast,
renin is high.
Congenital adrenal hyperplasia is a single causal chain.
A blocked enzyme lowers cortisol, feedback is lost,
ACTH rises and drives hyperplasia, and stranded precursors are diverted towards androgens.
Only 21- and 11-hydroxylase deficiencies virilise,
and only 11-
and 17-hydroxylase deficiencies raise blood pressure. 21-hydroxylase deficiency accounts for over 90 per cent,
with raised 17-hydroxyprogesterone, virilised female infants,
salt-wasting crisis in the first weeks
and low blood pressure. 11-beta-hydroxylase deficiency retains salt through deoxycorticosterone,
whereas 17-alpha-hydroxylase deficiency adds absent sexual development.
The adrenal cortex is organised into functionally distinct zones:
the outer glomerulosa produces aldosterone,
the fasciculata produces cortisol and the reticularis produces androgens;
catecholamines originate in the separate medulla.